scholarly journals The effect of platelet concentrate storage temperature on adenine nucleotide metabolism

Blood ◽  
1975 ◽  
Vol 45 (6) ◽  
pp. 749-756
Author(s):  
DJ Filip ◽  
JD Eckstein ◽  
CA Sibley
Keyword(s):  
Storage Temperature ◽  
Adenine Nucleotide ◽  
Nucleotide Metabolism ◽  
Platelet Concentrate ◽  
Release Reaction ◽  
C Storage ◽  
Adenine Nucleotide Metabolism ◽  
Red Cell Count ◽  
Ph Decrease ◽  
Adenine Nucleotide Pool

The effect of platelet concentrate storage temperature (4 degrees C versus 22 degrees C) on platelet adenine nucleotide metabolism was studied. In general, levels of platelet ATP and ADP, the release reaction, and the metabolis nucleotide pool were best preserved for 72 hr by storage of concentrates at 4 degrees C. Storage of concentrates for 72 hr at 22 degrees C was occasionally associated with a pH decrease to less than 6.0, which is incompatible with platelet viability. When the pH fell below 6.0, there was a marked deterioration of platelet adenine nucleotide levels and the release reaction. The results for concentrates stored at 22 degrees C, with a final pH above 6.0, were not inferior to the results for those stored at 4 degrees C. The pH remained above 7.0 in all concentrates stored at 4 degrees C. The pH changes of platelet concentrates stored at 22 degrees C could not solely be attributed to platelet count, red cell count, or bacterial contamination. Storage at both temperatures was associated with conversion of ATP in the metabolic adenine nucleotide pool to hypoxanthine.

scholarly journals The effect of platelet concentrate storage temperature on adenine nucleotide metabolism

Blood ◽  
1975 ◽  
Vol 45 (6) ◽  
pp. 749-756 ◽  
Author(s):  
DJ Filip ◽  
JD Eckstein ◽  
CA Sibley
Keyword(s):  
Storage Temperature ◽  
Adenine Nucleotide ◽  
Nucleotide Metabolism ◽  
Platelet Concentrate ◽  
Release Reaction ◽  
C Storage ◽  
Adenine Nucleotide Metabolism ◽  
Red Cell Count ◽  
Ph Decrease ◽  
Adenine Nucleotide Pool

Abstract The effect of platelet concentrate storage temperature (4 degrees C versus 22 degrees C) on platelet adenine nucleotide metabolism was studied. In general, levels of platelet ATP and ADP, the release reaction, and the metabolis nucleotide pool were best preserved for 72 hr by storage of concentrates at 4 degrees C. Storage of concentrates for 72 hr at 22 degrees C was occasionally associated with a pH decrease to less than 6.0, which is incompatible with platelet viability. When the pH fell below 6.0, there was a marked deterioration of platelet adenine nucleotide levels and the release reaction. The results for concentrates stored at 22 degrees C, with a final pH above 6.0, were not inferior to the results for those stored at 4 degrees C. The pH remained above 7.0 in all concentrates stored at 4 degrees C. The pH changes of platelet concentrates stored at 22 degrees C could not solely be attributed to platelet count, red cell count, or bacterial contamination. Storage at both temperatures was associated with conversion of ATP in the metabolic adenine nucleotide pool to hypoxanthine.

Muscle adenine nucleotide metabolism during and in recovery from maximal exercise in humans

2000 ◽  
Vol 88 (5) ◽  
pp. 1513-1519 ◽  
Author(s):  
S. Zhao ◽  
R. J. Snow ◽  
C. G. Stathis ◽  
M. A. Febbraio ◽  
M. F. Carey
Keyword(s):  
Adenine Nucleotide ◽  
Vastus Lateralis ◽  
Recovery Period ◽  
Nucleotide Metabolism ◽  
Peak Oxygen Consumption ◽  
Vastus Lateralis Muscle ◽  
Adenine Nucleotide Metabolism ◽  
Exercise Induced ◽  
Adenine Nucleotide Pool ◽  
The Relationship

The relationship between changes in the muscle total adenine nucleotide pool (TAN = ATP + ADP + AMP) and IMP during and after 30 s of sprint cycling was examined. Skeletal muscle samples were obtained from the vastus lateralis muscle of seven untrained men (23.9 ± 2.3 yr, 74.4 ± 3.6 kg, and 55.0 ± 2.9 ml ⋅ kg−1 ⋅ min−1peak oxygen consumption) before and immediately after exercise and after 5 and 10 min of passive recovery. The exercise-induced increase in muscle IMP was linearly related to the decrease in muscle TAN ( r = −0.97, P < 0.01), and the slope of this relationship (−0.83) was not different from 1.0 ( P > 0.05), indicating a 1:1 stoichiometric relationship. This interpretation must be treated cautiously, because all subjects displayed a greater decrease in TAN compared with the increase in IMP content, and the TAN + IMP + inosine + hypoxanthine content was lower ( P < 0.05) immediately after exercise compared with during rest. During the first 5 min of recovery, the increase in TAN was not correlated with the decrease in IMP ( r = −0.18, P> 0.05). In all subjects, the magnitude of TAN increase was higher than the magnitude of IMP decrease over this recovery period. In contrast, the increase in TAN was correlated with the decrease in IMP throughout the second 5 min of recovery ( r = −0.80, P < 0.05), and it was a 1:1 stoichiometric relationship (slope = −1.12). These data indicate that a small proportion of the TAN pool was temporarily lost from the muscle purine stores during sprinting but was rapidly recovered after exercise.

scholarly journals The Effect of Cold on Platelets. III. Adenine Nucleotide Metabolism After Brief Storage at Cold Temperature

Blood ◽  
1973 ◽  
Vol 42 (4) ◽  
pp. 557-564 ◽  
Author(s):  
Herman E. Kattlove ◽  
Dorothy Mormino
Keyword(s):  
Connective Tissue ◽  
Prostaglandin E1 ◽  
Room Temperature ◽  
Adenine Nucleotide ◽  
Platelet Rich Plasma ◽  
Adenine Nucleotides ◽  
Nucleotide Metabolism ◽  
Immunoglobulin M ◽  
Release Reaction ◽  
Adenine Nucleotide Metabolism

Abstract The effect of cold on platelet adenine nucleotide (PAN) metabolism was studied. Spontaneous aggregation which occurs when chilled platelet-rich plasma (PRP) is simultaneously warmed and stirred was not accompanied by the changes in adenine nucleotides associated with the release reaction. Connective tissue caused the release of the same amount of ADP and conversion of equal amounts of ATP to IMP and hypoxanthine in cold-stored platelets as it did in room temperature stored platelets. However, cold did have an important effect on PAN. In PRP stored at cold (0° C, 3° C) temperatures and warmed up to 37° C in the presence of 3H adenine, there was an increase in the conversion of adenine to its metabolites and ultimately to hypoxanthine as compared to PRP stored at warmer temperatures. This effect could not be prevented by ouabain, prostaglandin E1, antibody to immunoglobulin M or adenosine.

scholarly journals Studies on the mechanism of ristocetin-induced platelet aggregation

Blood ◽  
1975 ◽  
Vol 45 (1) ◽  
pp. 91-96 ◽  
Author(s):  
HE Kattlove ◽  
MH Gomez
Keyword(s):  
Platelet Aggregation ◽  
Adenine Nucleotide ◽  
Nucleotide Metabolism ◽  
Release Reaction ◽  
Platelet Membranes ◽  
Adenine Nucleotide Metabolism ◽  
Induced Aggregation

Abstract Adenine nucleotide metabolism and the release reaction were studied during ristocetin-induced platelet aggregation. Decreasing platelet ATP by incubation with metabolic poisons did not decrease ristocetin- induced aggregation. ADP and ATP were released from platelets during ristocetin-induced aggregation, and ATP was converted to hypoxanthine. However, these occurred after aggregation was almost complete. Aggregation was inhibited by p-choromercuribenzoic acid. By studying platelet suspensions, we were able to determine that this effect was on platelets and not on the plasma cofactor needed for aggregation. We postulate that ristocetin and its cofactor aggregate platelets by binding platelet membranes and that the platelet plays a passive role in this reaction.

scholarly journals Studies on the mechanism of ristocetin-induced platelet aggregation

Blood ◽  
1975 ◽  
Vol 45 (1) ◽  
pp. 91-96
Author(s):  
HE Kattlove ◽  
MH Gomez
Keyword(s):  
Platelet Aggregation ◽  
Adenine Nucleotide ◽  
Nucleotide Metabolism ◽  
Release Reaction ◽  
Platelet Membranes ◽  
Adenine Nucleotide Metabolism ◽  
Induced Aggregation

Adenine nucleotide metabolism and the release reaction were studied during ristocetin-induced platelet aggregation. Decreasing platelet ATP by incubation with metabolic poisons did not decrease ristocetin- induced aggregation. ADP and ATP were released from platelets during ristocetin-induced aggregation, and ATP was converted to hypoxanthine. However, these occurred after aggregation was almost complete. Aggregation was inhibited by p-choromercuribenzoic acid. By studying platelet suspensions, we were able to determine that this effect was on platelets and not on the plasma cofactor needed for aggregation. We postulate that ristocetin and its cofactor aggregate platelets by binding platelet membranes and that the platelet plays a passive role in this reaction.

scholarly journals Adenine nucleotide metabolism in isolated chicken hepatocytes

1987 ◽  
Vol 242 (2) ◽  
pp. 551-558 ◽  
Author(s):  
J Spychała ◽  
G Van den Berghe
Keyword(s):  
Uric Acid ◽  
Metabolic Flux ◽  
De Novo ◽  
Adenine Nucleotide ◽  
Adenine Nucleotides ◽  
Total Concentration ◽  
Nucleotide Metabolism ◽  
Adenosine Kinase ◽  
Adenine Nucleotide Metabolism ◽  
Adenine Nucleotide Pool

The turnover of the adenine nucleotide pool, the pathway of the degradation of AMP and the occurrence of recycling of adenosine were investigated in isolated chicken hepatocytes, in which the adenylates had been labelled by prior incubation with [14C]adenine. Under physiological conditions, 85% of the IMP synthesized by the ‘de novo’ pathway (approx. 37 nmol/min per g of cells) was catabolized directly via inosine into uric acid, and 14% was converted into adenine nucleotides. The latter were found to turn over at the rate of approx. 5 nmol/min per g of tissue. Inhibition of adenosine deaminase by 1 microM-coformycin had no effect on the formation of labelled uric acid, indicating that the initial degradation of AMP proceeds by way of deamination rather than dephosphorylation. Inhibition of adenosine kinase by 100 microM-5-iodotubercidin resulted in a loss of labelled ATP, demonstrating that adenosine is normally formed from AMP but is recycled. Unexpectedly, 5-iodotubercidin did not decrease the total concentration of ATP, indicating that the loss of adenylates caused by inhibition of adenosine kinase was nearly completely compensated by formation of AMP de novo. Anoxia induced a greatly increased catabolism of the adenine nucleotide pool, which proceeded in part by dephosphorylation of AMP. On reoxygenation, the formation of AMP de novo was increased 8-fold as compared with normoxic conditions. The latter results indicate the existence of adaptive mechanisms in chick liver allowing, when required, channelling of the metabolic flux through the ‘de novo’ pathway, away from the uricotelic catabolic route, into the synthesis of adenine nucleotides.

The Platelet of the Newborn Infant – Adenine Nucleotide Metabolism and Release

1980 ◽  
Vol 43 (02) ◽  
pp. 099-103 ◽  
Author(s):  
J M Whaun ◽  
P Lievaart ◽  
Keyword(s):  
Newborn Infant ◽  
Adenine Nucleotide ◽  
Platelet Rich Plasma ◽  
Adenine Nucleotides ◽  
Newborn Infants ◽  
Specific Radioactivity ◽  
Nucleotide Metabolism ◽  
Breakdown Product ◽  
Term Infants ◽  
Adenine Nucleotide Metabolism

SummaryBlood from normal full term infants, mothers and normal adults was collected in citrate. Citrated platelet-rich plasma was prelabelled with 3H-adenine and reacted with release inducers, collagen and adrenaline. Adenine nucleotide metabolism, total adenine nucleotide levels and changes in sizes of these pools were determined in platelets from these three groups of subjects.At rest, the platelet of the newborn infant, compared to that of the mother and normal adult, possessed similar amounts of adenosine triphosphate (ATP), 4.6 ± 0.2 (SD), 5.0 ± 1.1, 4.9 ± 0.6 µmoles ATP/1011 platelets respectively, and adenosine diphosphate (ADP), 2.4 ± 0.7, 2.8 ± 0.6, 3.0 ± 0.3 umoles ADP/1011 platelets respectively. However the marked elevation of specific radioactivity of ADP and ATP in these resting platelets indicated the platelet of the neonate has decreased adenine nucleotide stores.In addition to these decreased stores of adenine nucleotides, infant platelets showed significantly impaired release of ADP and ATP on exposure to collagen. The release of ADP in infants, mothers, and other adults was 0.9 ± 0.5 (SD), 1.5 ± 0.5, 1.5 ± 0.1 umoles/1011 platelets respectively; that of ATP was 0.6 ± 0.3, 1.0 ± 0.1,1.3 ± 0.2 µmoles/1011 platelets respectively. With collagen-induced release, platelets of newborn infants compared to those of other subjects showed only slight increased specific radioactivities of adenine nucleotides over basal levels. The content of metabolic hypoxanthine, a breakdown product of adenine nucleotides, increased in both platelets and plasma in all subjects studied.In contrast, with adrenaline as release inducer, the platelets of the newborn infant showed no adenine nucleotide release, no change in total ATP and level of radioactive hypoxanthine, and minimal change in total ADP. The reason for this decreased adrenaline reactivity of infant platelets compared to reactivity of adult platelets is unknown.Infant platelets may have different membranes, with resulting differences in regulation of cellular processes, or alternatively, may be refractory to catecholamines because of elevated levels of circulating catecholamines in the newborn period.

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